Naked Science Forum
Life Sciences => Cells, Microbes & Viruses => Topic started by: HDCantrell on 23/11/2010 20:30:02
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HDCantrell asked the Naked Scientists:
Chris, if you needed to answer this with something brilliant what would you answer??
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Thank you,
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In Christ
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HDCantrell
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Herbie is a typical American college freshman who loves to eat. His second most favorite food is hotdogs. He cuts them into his Kraft macaroni and cheese at a 1:1 ratio, going through a score of hotdogs each week. He doesn't know his brand is preserved with sodium nitrite, but his stomach is slowly finding out as it's acid converts the sodium nitrite to nitrous acid, a weak mutagen. In the lining of Herbie's stomach three little cells each experience a mutation in their DNA and it happens to be in the very same gene--a kinase gene called src. (Src is an example of what Dr. Howard Temin called a "proto-oncogene.)
But the three little cells each experienced a different kind of mutation in that gene:
Cell #1's src DNA was altered so that it's product is present in normal amounts, but no longer functions.
Cell #2's src DNA was altered so that it produces almost no gene product at all.
Cell #3's src DNA was altered so that it's gene product has normal function but is overproduced.
Workers have long known that mutations cause cancer. A mutagen (substance or form of energy that causes mutations) is usually a carcinogen (substance or form of energy that causes cancer).
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Which of the three cells above is more likely to become cancerous?
What do you think?
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It would certainly depend on the genes involved.
There are some "error correction" genes, that if they were not fully expressed, they would lead to a higher probability of additional mutations not being detected, and thus could lead to cancers.
There are some genes that get activated that should not be activated in a particular cell line, for example the genes in macrophages that allow movement and migration can be particularly damaging with respect to cancer.
There are some genes that become hyperactive, such as those that would be regulating cell replication that can lead to uncontrolled tumor growth.
One theory is that some cancers are caused by a natural lack of telomerase, which causes an eventual loss of the telomeres, and eventually important genes being deleted. Supplying an unlimited supply of telomerase might actually prevent these cancers.
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Cell #1's src DNA was altered so that it's product is present in normal amounts, but no longer functions.
Cell #2's src DNA was altered so that it produces almost no gene product at all.
Cell #3's src DNA was altered so that it's gene product has normal function but is overproduced.
Cell 1-Protein misfolding leading to loss of function.
Cell 2-Loss of function
Cell 3-Gain of function
Src is a protein specific tyrosine kinase, so depending on what it was phosphorylating, and which pathway it lead into would be dependant on how a mutation would act on it. What would it increase? Decrease? How does that act further on in the transduction pathway.Have a think about it.... [;)]
Tumour promoters act synergistically with mutagens/carcinogens, it is not an all or nothing thing.